炎症
前列腺素E2
自噬
环氧合酶
免疫系统
前列腺素E
前列腺素
药理学
医学
细胞凋亡
免疫学
生物
酶
内科学
生物化学
作者
Zhanfei Chen,Rong Chen,L. Wang,Zihao Yu,W. Chen,Hua Lin,Liumin Yu,Jinqiu Li,Zhonghui Chen,Jianlin Shen,Nanhong Tang
标识
DOI:10.2174/0109298673327820241004042817
摘要
Abstract: Prostaglandin E2 (PGE2) plays a crucial role in inflammation. Non-steroidal anti-inflammatory medications are commonly utilized to alleviate pain and address inflammation by blocking the production of PGE2 and cyclooxygenase (COX). However, selective inhibition of COX can easily lead to a series of risks for cardiovascular diseases. Hence, it is imperative to discover safer and more efficient targets for reducing inflammation. Research has demonstrated that mPGES-1 serves as the final enzyme that controls the rate of prostaglandin E2 synthesis. Moreover, it is only triggered by inflammation and could serve as a possible treatment target instead of COX in cases of inflammation. 2,5-dimethylcelecoxib (DMC) can effectively inhibit mPGES-1 expression, maintain the overall balance of prostaglandins, reduce the secretion of PGE2, and, most importantly, avoid the side effects of COX inhibitors. DMC has the ability to address illnesses through the stimulation of autophagy and apoptosis, as well as the regulation of the immune microenvironment and intestinal flora. This study provides a comprehensive overview of the advancements in DMC within experimental research and offers suggestions for potential avenues of future investigation.
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